Another helpful summary of the recent paper linking jumping genes to cancer

A recent post discussed an important paper that demonstrated an association between transposable elements, aka ‘jumping genes’, and cancer. Transposable elements are an important but often forgotten class of mutagen that can contribute to genome instability and may disrupt genes and their expression. The original article has an outstanding abundance of data and is not easy reading. The article below provides an accessible summary that’s worth reading if you aren’t an expert in genomics.

Cancer: Scientists find 129 'jumping genes' that drive tumor growth

Catharine Paddock, Medical News Today

In cancer research, scientists usually look for cancer genes by scouring the genome for altered sequences — or mutations — in DNA. But a new study has now revealed that jumping genes, which customary sequencing overlooks, are also important drivers of tumor growth.

Scientists at the Washington University School of Medicine in St. Louis, MO, found that jumping genes are widespread in cancer and promote tumor growth by forcing cancer genes to remain switched on.

They analyzed 7,769 tumor samples from 15 different types of cancer and found 129 jumping genes that can drive tumor growth through their influence on 106 different cancer genes.

The jumping genes were functioning as "stealthy on-switches" in 3,864 of the tumors that the team analyzed. These tumors came from breast, colon, lung, skin, prostate, brain, and other types of cancer.

A recent Nature Genetics paper gives a full account of the study.

Small transposable elements can have big effects on genome size

Genome Size Evolution: Small Transposons with Large Consequences

Alexander Suh

Current Biology (Dispatch)

"Transposable elements (TEs) heavily influence genome size variation between organisms. A new study on larvacean tunicates now shows that even non-autonomous TEs — small TEs that parasitize the enzymatic machinery of large, autonomous TEs — can have a large impact on genome size.”

Highlights

•Genome size varies up to 12× in larvaceans, chordates with a distinctive anatomy

•Small and large species have the smallest and largest genomes, respectively

•Transposable elements have driven multiple independent genome expansions

•Genomes mainly increased through accumulations of non-autonomous elements (SINEs)

Summary—In eukaryotes, genome size correlates little with the number of coding genes or the level of organismal complexity (C-value paradox). The underlying causes of variations in genome size, whether adaptive or neutral, remain unclear, although several biological traits often covary with it . Rapid increases in genome size occur mainly through whole-genome duplications or bursts in the activity of transposable elements (TEs). The very small and compact genome of Oikopleura dioica, a tunicate of the larvacean class, lacks elements of most ancient families of animal retrotransposons . Here, we sequenced the genomes of six other larvaceans, all of which are larger than that of Oikopleura (up to 12 times) and which increase in size with greater body length. Although no evidence was found for whole-genome duplications within the group of species, the global amount of TEs strongly correlated with genome size. Compared to other metazoans, however, the TE diversity was reduced in all species, as observed previously in O. dioica, suggesting a common ancestor with a compacted genome. Strikingly, non-autonomous elements, particularly short interspersed nuclear elements (SINEs), massively contributed to genome size variation through species-specific independent amplifications, ranging from 3% in the smallest genome up to 49% in the largest. Variations in SINE abundance explain as much as 83% of interspecific genome size variation. These data support an indirect influence of autonomous TEs on genome size via their ability to mobilize non-autonomous element

READ HERE… for a summary and here for the original article.

‘Jumping genes’ drive many cancers

‘Jumping genes’ drive many cancers

Mistakes in DNA are known to drive cancer growth. But a new study, from Washington University School of Medicine in St. Louis, heavily implicates a genetic phenomenon commonly known as “jumping genes” in the growth of tumors.

The study is published March 29 in the journal Nature Genetics.

Since jumping genes aren’t mutations — mistakes in the letters of the DNA sequence — they can’t be identified by traditional cancer genome sequencing. As such, this study opens up new lines of research for future cancer therapies that might target such genes.

Jumping genes, which scientists call transposable elements, are short sections of the DNA sequence that have been incorporated randomly into the genome over the long course of human evolution. The evolutionary histories of jumping genes are the subject of much current research, but viral infection is thought to play an important role in their origins.

Researchers led by Ting Wang, PhD, the Sanford C. and Karen P. Loewentheil Distinguished Professor of Medicine, have plumbed genomic databases, looking specifically for tumors whose jumping genes are driving cancer growth.

READ MORE …